Phenol exerts a general bactericidal effect because of the compound's ability to partition into cell membranes, which leads to a loss of cytoplasmic membrane integrity. Phenol toxicity results in disruption of microbial activities associated with energy transformations, membrane barrier functions, and membrane protein functions, and causes eventual cell death. Nevertheless, microorganisms are known to develop mechanisms to resist and survive phenol at concentrations that are normally inhibitory to micro-bial activity. These mechanisms include isomerization of cis-unsaturated fatty acids to the trans--configuration and increase in proportion of saturated fatty acids to unsaturated fatty acids. Such adaptive responses to phenol exposure allow for chains of fatty acid molecules to be more closely aligned to improve the structural rigidity of cell membranes, thus compensating for the increased membrane fluidity induced by phenol partitioning (Heipieper et al., 1991; Keweloh et al., 1991; Yap et al., 1999). In fact, several mechanisms that decrease membrane fluidity in response to substrate toxicity have been proposed for Pseudomonas putida (Heipieper et al., 1992), Escherichia coli (Keweloh et al., 1991), and Vibrio species (Okuyama et al., 1991). Bacteria that possess such resistance mechanisms to counteract high concentrations of phenol would therefore be of considerable practical interest for deployment in biodegradation processes where phenolic compounds can exert a toxic or inhibitory effect.
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